左乙拉西坦对小鼠脑缺血再灌注损伤后Bax、Caspase-3表达的影响分析

Influence of Levamisetan on the expression of Bax and Caspase-3 in mouse with brain ischemia-reperfusion injury

目的探讨左乙拉西坦对小鼠脑缺血再灌注损伤后B淋巴细胞瘤-2基因相关X蛋白(Bax)、胱天蛋白酶3(Caspase-3)表达的影响。方法 2018年3月选取清洁级雄性健康成年小鼠105只,随机分为A组、B组与C组,A组15只,B组与C组各45只。A组进行假手术操作,B组制备脑缺血再灌注模型,B组和C组进一步分为3个亚组,其亚组各15只。在建立模型后0 h、3 h、6 h C组分别使用左乙拉西坦10 mg/kg尾静脉注射,B组注射0.9%氯化钠溶液。对比三组神经功能评分、脑梗死体积、凋亡指数、Bax、Caspase-3表达情况。结果三组神经功能评分比较:C组较A组高,较B组评分低(P<0.05);C组脑梗死体积在建模后0 h、3 h、6 h时均低于B组(P<0.05),C组随着建模时间延长,给药越晚脑梗死体积越大(P<0.05);B组和C组小鼠脑组织凋亡指数、Bax、Caspase-3表达均明显高于A组(P<0.05),C组小鼠脑组织凋亡指数、Bax、Caspase-3在建模后0 h、3 h、6 h时均低于B组(P<0.05),C组随着建模时间延长,给药越晚,脑组织晚凋亡指数越大,Caspase-3表达含量越高(P<0.05),Bax表达差异无显著性(P>0.05)。结论左乙拉西坦对小鼠脑缺血再灌注损伤后Bax、Caspase-3表达具有抑制作用,可抑制脑组织神经细胞凋亡,具有脑保护作用。在小鼠缺血再灌注3 h内应用左乙拉西坦抑制脑组织神经细胞凋亡疗效最佳。

Objective To discusses influence of Levamisetan on the expression of Bax and Caspase-3 in mouse with brain ischemia-reperfusion injury. Methods 105 clean level healthy adult male mice were randomly divided into group A 15 mice,group B and group C 45 mice in each group. Group A was given sham operation,group B was given preparation of cerebral ischemia reperfusion model. Groups B and C were divided into 3 subgroups with 15 mice in each subgroup. Group C after model established were given tail vein injection with levamisetan in 0 h,3 h,6 h,B group was injected with 0. 9% sodium chloride solution. The nerve function score,cerebral infarction volume,apoptosis index,Bax,Caspase-3 expression were compared among groups. Results The nerve function score comparison： group C was higher than group A,group C was lower than group B（ P〈0. 05）; Group C after cerebral infarction volume in modeling 0 h,3 h,6 h were lower than that of group B（ P〈0. 05）,group C as the modeling time prolonged,the late for cerebral infarction volume was larger（ P〈0. 05）; Brain tissue apoptosis index,Bax,Caspase-3 expression in Group B and group C mice were significantly higher than those of group A（ P〈0. 05）,Brain tissue apoptosis index,Bax,Caspase-3 of group C mice in modeling after 0 h,3 h,6 h were lower than those of group B（ P〈0. 05）,group C as the modeling time prolonged,the longer,the greater the brain tissue apoptosis index,Caspase-3 expression level was higher（ P〈0. 05）,the expression of Bax had no significant difference（ P〈0. 05）. Conclusion Levetiracetam can inhibit the expression of Bax and Caspase-3 after cerebral ischemia-reperfusion injury in mice,can inhibit apoptosis of brain tissue,with brain protection. The efficacy of levetiracetam in inhibiting neuronal apoptosis in brain tissue is best within 3 h after ischemia-reperfusion in mice.